Hypernatremia is common in the intensive care setting, with a prevalence of up to 25%. It is linked with longer hospital stays and is an independent risk factor for mortality. The present study described a case of hypernatremia of multifactorial origin in the intensive care setting, emphasizing the role of osmotic diuresis due to excessive urea generation, which is an underdiagnosed and often ignored cause of hypernatremia. 

It describes a case of a 72-year-old woman with a previous medical history of hypertension, type 2 diabetes mellitus, and heart failure who presented with hypertensive acute pulmonary edema requiring invasive mechanical ventilation. 

Electrocardiogram revealed a left bundle branch block. However, markers were negative for myocardial necrosis, and cardiac catheterization did not indicate significant obstructions. 

She was extubated on the fourth day of hospitalization but showed severe laryngospasm refractory to clinical measures, as corticoid therapy, requiring reintubation. Subsequently, she developed ventilator-associated pneumonia and increased serum sodium level (165 mEq/L). 

She received 0.45% NaCl solution and free water through a nasoenteric feeding tube without improvement of natremia. Signs of congestion on chest radiography, peripheral edema, and oliguria prompted the initiation of 40 mg/day of intravenous furosemide. 

Further, during the ventilator weaning process, she showed right hemiparesis. Cranial computed tomography showed a hemorrhagic stroke in the left middle cerebral artery region. After extubation, she remained with aphasia and dysphagia, persisting with the need for an enteral diet. 

On the 14th day of hospitalization, the patient was clinically hypervolemic, tending to hypertension, with an accumulated positive fluid balance despite diarrhea and febrile condition and urine volume (UV) of around two liters/day. She was still on high doses of intravenous corticosteroid (methylprednisolone 75 mg 8/8h), initially prescribed due to laryngospasm. Her furosemide was discontinued on the 12th day of hospitalization due to worsening renal function and hypernatremia. She received an enteral diet as- diet for a diabetic patient, volume per day = 1,500 mL, hyperproteic (75 g/L), with osmolarity of 530 mOsm/L, and sodium concentration of 17 mEq/L. As per her 60 kg weight, she received 1.8 g/kg of protein.

Her laboratory investigations showed- 

• free water clearance (CH2O) = - 1,320 mL;
• electrolyte-free water clearance (CeH2O) = + 957 mL;
• total urine osmoles = 1,154 mOsm;
• urine osmoles generated by urea = 814 mOsm;
• urine osmoles generated by Na + K = 340 mOsm. 

Based on these results, she received the diagnosis of hypernatremia induced by osmotic diuresis secondary to excessive urea generation.

After diagnosis, her protein supply of the enteral diet was reduced to 1.0 g/kg, and corticosteroid doses were tapered. Five days following these, her urinary urea decreased to 24.6 g/day, corresponding to 410 mOsm of the total of 875 mOsm in the urine, correcting the previous osmotic effect induced by excessive urea generation. Likewise, she also showed a progressive decrease in plasma urea and sodium levels.

This kind of scenario may appear in patients using high doses of corticosteroids, with gastrointestinal bleeding, under diets and hyper protein supplements, and with hypercatabolism, particularly during the recovery phase of renal injury. The recognition of CeH2O is the cornerstone for its diagnosis.

J Bras Nefrol. 2020 Mar;42(1):106-112. doi: 10.1590/2175-8239-JBN-2018-0226. Epub 2019 Apr 25. PMID: 31063175; PMCID: PMC7213928.